BACKGROUND: Intercellular adhesion molecule-1 (ICAM-1) plays an important role in immune responses, especially in T cell/endothelial cell and T cell/macrophage interactions. This study reports the cellular localization of ICAM-1 during immune-mediated demyelination of the peripheral nervous system induced by adoptive transfer of P2 specific T cells. EXPERIMENTAL DESIGN: Cryosections 1 micron thick of ventral roots of rats with experimental autoimmune neuritis were labeled with a monoclonal antibody against rat ICAM-1. RESULTS: Numerous ICAM-1 positive cells were present before and shortly after the onset of clinical disease from days 4 to 6 after cell transfer. By day 8, their number had greatly decreased. ICAM-1 positive infiltrating cells could be identified as ED1 positive macrophages. Moreover, endothelial cells expressed ICAM-1. Schwann cells and T cells were ICAM-1 negative. While at early stages of experimental autoimmune neuritis, ICAM-1 and Ia colocalized on macrophages but not endothelial cells, Ia persisted for a longer period in nerve roots than ICAM-1. After nerve transection, macrophages entering the distal stump and endothelial cells did not express ICAM-1. CONCLUSIONS: The presence of ICAM-1 immunoreactivity in peripheral nerve indicates an underlying immune-mediated process. Among other cytokines interferon-gamma, which is transiently expressed in nerves during immune-mediated demyelination but not after nerve transection, could be one mediator that induces ICAM-1 in immune-mediated demyelination of the peripheral nervous system.
BACKGROUND:Intercellular adhesion molecule-1 (ICAM-1) plays an important role in immune responses, especially in T cell/endothelial cell and T cell/macrophage interactions. This study reports the cellular localization of ICAM-1 during immune-mediated demyelination of the peripheral nervous system induced by adoptive transfer of P2 specific T cells. EXPERIMENTAL DESIGN: Cryosections 1 micron thick of ventral roots of rats with experimental autoimmune neuritis were labeled with a monoclonal antibody against ratICAM-1. RESULTS: Numerous ICAM-1 positive cells were present before and shortly after the onset of clinical disease from days 4 to 6 after cell transfer. By day 8, their number had greatly decreased. ICAM-1 positive infiltrating cells could be identified as ED1 positive macrophages. Moreover, endothelial cells expressed ICAM-1. Schwann cells and T cells were ICAM-1 negative. While at early stages of experimental autoimmune neuritis, ICAM-1 and Ia colocalized on macrophages but not endothelial cells, Ia persisted for a longer period in nerve roots than ICAM-1. After nerve transection, macrophages entering the distal stump and endothelial cells did not express ICAM-1. CONCLUSIONS: The presence of ICAM-1 immunoreactivity in peripheral nerve indicates an underlying immune-mediated process. Among other cytokines interferon-gamma, which is transiently expressed in nerves during immune-mediated demyelination but not after nerve transection, could be one mediator that induces ICAM-1 in immune-mediated demyelination of the peripheral nervous system.